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Dinitrochlorobenzene is genotoxic by sister chromatid exchange in human skin fibroblasts

L D DeLeve1

  • 1Department of Pharmacology, Hospital for Sick Children, Toronto, Ont., Canada. deleve@hsc.usc.edu

Mutation Research
|November 4, 1996
PubMed

Insights

Dinitrochlorobenzene (DNCB) shows genotoxicity in human skin cells, increasing sister chromatid exchange at low concentrations. This finding necessitates careful consideration of its clinical use versus potential long-term toxicity risks.

Area of Science:

  • Toxicology
  • Dermatology
  • Genetics

Background:

  • Dinitrochlorobenzene (DNCB) is an effective treatment for alopecia areata.
  • Previous mutagenicity findings in the Ames test limited DNCB's clinical application.
  • Renewed interest exists for DNCB's immunomodulatory effects in HIV and lupus erythematosus patients.

Purpose of the Study:

  • To investigate the genotoxicity of DNCB in human skin fibroblasts.
  • To evaluate DNCB's potential to induce sister chromatid exchange (SCE).

Main Methods:

  • Human skin fibroblasts were exposed to varying concentrations of DNCB.
  • Sister chromatid exchange assay was performed to assess genotoxicity.

Main Results:

  • DNCB significantly increased sister chromatid exchange in human skin fibroblasts.
  • Genotoxicity was observed at concentrations from 2.5 to 10 microM.
  • These effective concentrations are below those typically used in clinical settings.

Conclusions:

  • Dinitrochlorobenzene is genotoxic to human skin fibroblasts at clinically relevant concentrations.
  • The potential risks of DNCB genotoxicity must be balanced against its therapeutic benefits for severe conditions.

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